Diagnosis: Subclinical Hyperthyroidism

The diagnosis is subclinical hyperthyroidism, defined by a suppressed TSH (0.008 mIU/L, which is <0.1 mIU/L) with normal free T4 and T3 levels. 1

Classification and Severity

This patient has Grade II subclinical hyperthyroidism (TSH <0.1 mIU/L), which represents a more significant degree of TSH suppression than Grade I (TSH 0.1-0.45 mIU/L). 2
The normal T3 and T4 levels distinguish this from overt hyperthyroidism, which would show elevated thyroid hormone levels in addition to suppressed TSH. 3, 4

Endogenous causes:

Exogenous and other causes:

Excessive levothyroxine replacement therapy (if patient is on thyroid hormone) 1, 3
Recovery phase after treatment for hyperthyroidism 1, 3
Medications: dopamine, glucocorticoids, or dobutamine 1, 3
Nonthyroidal illness (euthyroid sick syndrome), though undetectable TSH (<0.01 mIU/L) is rare without concomitant glucocorticoids or dopamine 1

Despite the absence of symptoms, this condition carries important long-term risks:

Increased risk of atrial fibrillation and cardiac arrhythmias, particularly in elderly patients 3, 4
Potential increased cardiovascular mortality 3

Bone mineral density loss, especially in postmenopausal women 1, 3
Increased fracture risk at hip and spine in women older than 65 years with TSH ≤0.1 mIU/L 1
Two studies demonstrated significant continued bone loss in untreated postmenopausal women with TSH <0.1 mIU/L compared to treated patients 1

1-2% per year risk of progression to overt hyperthyroidism in patients with TSH <0.1 mIU/L 1
This is substantially higher than the progression risk for those with TSH 0.1-0.45 mIU/L, where few progress to overt disease 1, 5
One study found incidence rates of 29.63 cases per 100 patient-years for TSH <0.10 mU/L versus only 4.12 cases per 100 patient-years for TSH 0.30-0.49 mU/L 5

Immediate next steps:

Repeat thyroid function tests within 4 weeks to confirm persistent TSH suppression, including TSH, free T4, and total T3 or free T3. 1, 3
- If the patient has cardiac disease, atrial fibrillation, or other serious medical conditions, repeat testing within 2 weeks instead 1, 3
Obtain detailed medication history to rule out exogenous causes, particularly levothyroxine, dopamine, or glucocorticoids. 1, 3
Establish the etiology with imaging:
- Radioactive iodine uptake and scan to distinguish between Graves' disease, toxic nodular goiter, and destructive thyroiditis 1, 3
- Thyroid ultrasonography to evaluate for nodules 3
Consider TSH receptor antibody testing if clinical features suggest Graves' disease (though typically more symptomatic). 1

For confirmed subclinical hyperthyroidism with TSH <0.1 mIU/L:

Treatment should be strongly considered given the TSH level is <0.1 mIU/L, even in asymptomatic patients, particularly if the patient is elderly, postmenopausal female, or has cardiac or bone disease risk factors. 1
Treatment options depend on etiology and include antithyroid drugs, radioactive iodine, or surgery. 1, 4
If observation is chosen (in younger patients without risk factors), close monitoring at 3-12 month intervals is required until TSH normalizes or the condition is confirmed stable. 1, 3

Do not dismiss this as clinically insignificant simply because the patient is asymptomatic—the risks of atrial fibrillation, fractures, and progression to overt disease are real. 1, 3, 4
Do not overlook medication-induced causes, particularly if the patient is on levothyroxine, dopamine, or glucocorticoids. 1, 3
Warn patients with nodular thyroid disease about iodine exposure (e.g., radiographic contrast agents), which may precipitate overt hyperthyroidism. 1, 3
Do not rely on T3 levels to exclude over-replacement in patients on levothyroxine—normal T3 can be seen in over-replaced patients. 6
Distinguish from central hypothyroidism, where both TSH and free T4 would be low (not the case here). 1